Diabetes mellitus is a chronic disorder in human and responsible for different complications and also causes mortality and morbidity. A wide number of herbal products are employed in the treatment of diabetes for their better efficacy and safety compared to synthetic medicine. The present studies have established the antidiabetic potential and rejuvenating capacity of kidney tissues under the effect of extract. Diabetes was induced in the Swiss albino mice by injecting alloxan at the dose of 150？mg/kg body weight and aqueous extract of Momordica charantia fruits at doses of 100？mg/kg body weight and 250？mg/kg body weight was administered orally for three weeks. After 21 days of treatment of the aqueous extracts of Momordica charantia significantly reduces serum glucose level, kidney function tests, lipid peroxidation as well as histopathological study also did show adverse alternation in the morphological architecture of the kidney tissue. Thus, from this study we concluded that Momordica charantia exhibited significant antihyperglycemic and rejuvenating capacity of kidney tissues activities in alloxan induced diabetic mice. 1. Introduction Diabetes mellitus (DM) is possibly the world’s fastest growing metabolic disorder and as the knowledge of the heterogeneity of this disorder increases so does the need for more appropriate therapies [1]. DM is a pathologic condition, resulting in severe metabolic imbalances and nonphysiologic changes in many tissues, where oxidative stress plays an important role in the aetiology [1, 2]. Diabetes is associated with the generation of reactive oxygen species (ROS) which cause oxidative damage, particularly to heart, kidney, eyes, nerves, liver, small and large blood vessels, and immunological and gastrointestinal system [1, 3]. Diabetic nephropathy (DN) is one of the important microvascular complications of diabetes mellitus. Recent studies indicate that reactive oxygen species (ROS) play a key intermediate role in the pathophysiology of diabetic nephropathy [4]. Hyperglycaemia, the main determinant of the initiation and progression of diabetic nephropathy, not only generates more reactive oxygen metabolites but also attenuates antioxidative mechanisms through nonenzymatic glycosylation of antioxidant enzymes [1]. The mechanism by which hyperglycaemia causes free radical generation and thus causes oxidative stress is complex. High glucose concentration directly increases hydrogen peroxide production by murine mesangial cells and lipid peroxidation of glomeruli and glomerular mesangial cells [5]. Hyperglycaemia promotes
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